Our studies have demonstrated that alcohol abuse leads to a decrease in tissue levels of long chain polyunsaturated fatty acids like arachidonate(AA) and docosahexaenoate (DHA). For example, there is a selective decrease in the level of DHA in the livers of rhesus monkeys given alcohol on an ad libitum basis that was associated with the development of liver fibrosis after three years. Patients at the time of liver translplant with Alcoholic Liver Disease also showed a selective loss of DHA. There is also a loss of DHA in the brains and retinas of cats and rhesus monkeys after chronic alcohol exposure. It is hypothesized that the lowered level of these important cell membrane constituents leads to alterations in cellular function that may underlie some aspects of alcohol-induced organ injuries and that prevention or restoration of this decrement in essential fatty acids may be of therapeutic benefit to alcoholics. Progress has been made in understanding the underlying actions of alcohol on essential fatty acid metabolism. In studies of cats and rhesus monkeys exposed to chronic alcohol, there was a large increase in markers of lipid peroxidation. However, an increase in enrichment of long chain polyunsaturates, especially DHA, with deuterium supplied by the 18-carbon fatty acid precursors indicated that essential fatty acid formation and accretion in vivo was increased. This contention is opposite to the commonly held notion that alcohol inhibits desaturase enzymes. In a separate line of inquiry, the functional consequences of diets deficient in n-3 fatty acids have been studied in rats over three generations. A novel application to the field of essential fatty acid biology was made with the introduction of olfactory-based learning and memory-related tasks for brain function assessment. Our principal findings are that there is a poorer performance in the acquisition of olfactory set learning in rats where brain and olfactory bulb DHA was lowered thru dietary insufficiency. Spatial maze tasks including the water maze also indicated that animals with lower levels of brain DHA performed more poorly, swimming longer and at a higher rate, but finding the platform with a longer latency. Preliminary indications are that there is little or no difference in sensory capability with respect to olfaction. This work has important implications for human infant formula composition as it is currently devoid of DHA in North America thus leading to a decrease in infant brain DHA levels and suboptimal development and function.